Real-time polymerase chain reaction was used to show that the levels of mRNA expression for GRK2 were twice as high in the heart failure models compared to the controls.

Catecholamine release was examined from chromaffin cells taken from the adrenal glands. Chromaffin cells from the heart failure models did not inhibit the secretion of catecholamine, but an inhibitory effect was found in the control cells.

The inhibitor beta-adrenergic receptor kinase was used to inhibit GRK2 activity. This resulted in improved myocardial function.

Dr Walter Koch, professor of medicine and director of the centre for translational medicine at Jefferson Medical College, said: ‘If less catecholamine is presented to the heart, the beta receptors destabilise and that improves heart function.’

GRK2 inhibitors could make human gene therapy for heart failure possible, he said.